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Induction of the tobacco PR‐1a gene by virus infection and salicylate treatment involves an interaction between multiple regulatory elements
Author(s) -
Rhee Miranda D.,
Bol John F.
Publication year - 1993
Publication title -
the plant journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.058
H-Index - 269
eISSN - 1365-313X
pISSN - 0960-7412
DOI - 10.1111/j.1365-313x.1993.tb00012.x
Subject(s) - tobacco mosaic virus , heterologous , reporter gene , gene , promoter , response element , biology , negative regulatory element , transcription (linguistics) , heterologous expression , regulation of gene expression , regulatory sequence , gene expression , microbiology and biotechnology , genetics , virus , recombinant dna , linguistics , philosophy
Summary Expression of the tobacco PR‐1a gene is induced by treatment of plants with salicylate or infection with tobacco mosaic virus (TMV). Cis ‐acting sequences involved in regulation of the PR‐1a gene by salicylate and TMV were identified by investigating fusion constructs of PR‐1a upstream sequences with a heterologous minimal promoter and the GUS reporter gene in transformed tobacco plants. The PR‐1a promoter was found to contain a number of interacting elements which function in a context‐dependent way. A minimum of four regulatory elements was identified, located between nucleotides ‐902 to ‐691 (element 1), ‐689 to ‐643 (element 2), ‐643 to ‐287 (element 3) and ‐287 to +29 (element 4). Alone, these elements have no promoter activity and they are all four required for maximum induction of the reporter gene by salicylate or TMV. The PR‐1a promoter is positively regulated by elements 1, 2 , and 3 ; constructs containing two of these three elements had about half of the maximum activity. Replacement of the minimal heterologous promoter by element 4 differentially affected the activity of these various constructs, suggesting that this element may be important for a correct spacing between elements 1 to 3 and the transcription start site. The observation that all PR‐1a promoter constructs respond similarly to salicylate treatment and TMV infection supports a role of salicylate in the signal transduction pathway leading to PR‐1a gene expression.